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MINERVA ANESTESIOLOGICA

Rivista di Anestesia, Rianimazione, Terapia Antalgica e Terapia Intensiva


Official Journal of the Italian Society of Anesthesiology, Analgesia, Resuscitation and Intensive Care
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
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Minerva Anestesiologica 2014 August;80(8):933-41

lingua: Inglese

Mechanotransduction in the lungs

Spieth P. M. 1, Bluth T. 1, Gama De Abreu M. 1, Bacelis A. 2, Goetz A. E. 2, Kiefmann R. 2

1 Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden, Germany;
2 Department of Anesthesiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany


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Mechanical ventilation may induce or aggravate lung injury, a phenomenon known as ventilator induced lung injury (VILI). On a macroscopic level, the effects of mechanical stress and strain on lung tissue are well described. Increased tidal volumes may lead to volutrauma, raised airway pressures may cause barotrauma and cyclic collapse and reopening of alveolar units contributes to atelectrauma. These three harmful mechanisms may lead to local and systemic pulmonary inflammatory response known as biotrauma. The purpose of this review was to elucidate fundamental mechanisms involved in the mechanotransduction of mechanical stimuli on a cellular level. Bronchial epithelial cells in the distal airways as well as alveolar epithelial cells are exposed to a variety of mechanical forces. These cells are involved in sensing and translation of mechanical stimuli into an inflammatory response. This review provides insight into current knowledge of cellular and molecular pathways during the process of pulmonary epithelial mechanosensation and mechanotransduction under different mechanical conditions. Since evidence for specific pathways is generally lacking in some fields of alveolar epithelial mechanotransduction, this article aims at providing reasonable hypothesis for further investigation.

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peter.spieth@uniklinikum-dresden.de